Dr. Fisher is Director of the Marc and Ruti Bell Vascular Biology and Disease Program. His major areas of focus are mechanisms related to risk factors causing coronary artery disease. His group spans the range of cell-free systems to mouse models and use modern techniques of cellular and molecular biology. Recent papers have highlighted their work in novel pathways regulating hepatic lipoprotein secretion as well as atherosclerosis regression. In addition to the laboratory program, Dr. Fisher also lead a clinical research program in risk factor reduction. There are a number of funded studies in a number of areas of preventive cardiology (e.g., insulin resistance, hypertension, obesity, and HDL) that are being directed by colleagues in the Lipid Treatment and Research Center (Drs. Schwartzbard, Schloss, and Weintraub) or in collaboration with faculty in the Cardiac Catherization Laboratory (Dr. Michael Attubato).

Selected Publications:

1. S.M. Hofmann, H. Dong, Z. Li, W. Cai, J. Altomonte, S. Thung, F. Zeng, E.A.Fisher, and H. Vlassara. Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse. Diabetes 51:2082-2089, 2002
2. R. Choudhury, V. Fuster, J.J. Badimon, E.A. Fisher, and Z. Fayad. Magnetic resonance imaging and characterization of atherosclerotic plaque: emerging applications and molecular imaging. Arteriosc. Thromb. Vasc. Biol. 22:1065-1074, 2002
3. Christopher Cardozo, Xinye Wu, Hongxing Wang, and Edward A. Fisher. The inhibition of microsomal triglyceride transfer protein activity in rat hepatoma cells promotes proteasomal and non-proteasomal degradation of apoprotein B100. Biochemistry 41:10105-10114, 2002
4. J. Rong, J. Berman, M.B. Taubman, and E.A. Fisher. Lysophosphatidylcholine stimulates monocyte chemoattractant protein-1 expression in rat aortic smooth muscle cells. Arteriosc. Thromb. Vasc. Biol. 22:1617-23, 2002
5. Hsiao D. Lieu; Shannon K. Withycombe; Quinn Walker; James X. Rong; Rosemary L. Walzem; Jinny S. Wong; Robert L. Hamilton; Edward A. Fisher; and Stephen G. Young. Eliminating Atherogenesis in Mice by Switching off Hepatic Lipoprotein Secretion. Circulation 107:1315-21, 2003.
6. B. Feng, P.M. Yao, Y. Li, C.M. Devlin, D. Zhang, H.P. Harding, M. Sweeney, J.X., Rong, G. Kuriakose, E.A. Fisher, A.R. Marks, D. Ron, and I. Tabas. The endoplasmic reticulum as the site of cholesterol-induced cytotoxicity in macrophages. Nature Cell Biology 5:781-92, 2003.
7. Gusarova, V., Brodsky, J.L., and Fisher, E.A. Apolipoprotein B100 exit from the ER is COPII dependent and its lipidation to very low density lipoprotein occurs post ER. J. Biol. Chem 278:48051-8, 2003
8. Rong, JX, Shapiro, M, Trogan, E, and Fisher, E.A. Trans-differentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading. Proc. Natl. Acad. Sci. (USA) 100:13531-6, 2003
9. Pan, M, Cederbaum, AI, Zhang, YL, Ginsberg, HN, Williams, KJ, and Fisher, EA. Lipid peroxidation and oxidant stress regulate hepatic apolipoprotein B degradation and VLDL production. In press, J. of Clin. Invest., 2004.
10. Wientgen, H, Thorngate, FE, Omerhodzic, S, Rolnitzky, L, Fallon, JT, Williams, DL, and Fisher, EA. Sub-physiologic plasma levels of apoE inhibit neointimal formation after arterial injury in apoE-deficient mice. In press, Arter. Thromb. Vasc. Biol., 2004.
11. Llorda, J., Angeli, V., Liu, J., Trogan, E., Fisher, EA, and Randolph, GJ. Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques. In press, Proc. Natl. Acad. Sci. (USA), 2004.
12. Trogan, E., Fayad, ZA, Itskovich , V, Aguinaldo , JS, Mani , V; Fallon , JT, Chereshnev , I, and Fisher, EA. Serial studies of mouse atherosclerosis by in vivo magnetic resonance imaging detects lesion regression after correction of dyslipidemia. In press, Arter. Thromb. Vasc. Biol., 2004.
13. Robin P. Choudhury , James X. Rong, Eugene Trogan, Valerie I. Elmalem , Hayes M. Dansky, Jan L. Breslow, Joseph L. Witztum , John T. Fallon, and Edward A. Fisher. HDL retards the progression of atherosclerosis and favorably remodels lesions without suppressing indices of inflammation or oxidation. In press, Arter. Thromb. Vasc. Biol., 2004.
14. Angeli, V., Llorda, J., Rong, JX, Satoh, K., Ishii, S., Shimizu, T., Fisher, EA, and Randolph, GJ. Dyslipidemia associated with atherosclerotic disease systemically alters dendritic cell mobilization. In press, Immunity, 2004.